Effects of Artesunate prevent nephritis via the Toll-like receptor 4/nuclear factor-κB signaling pathway in rats
Author(s) -
Rong Wan,
Yue Hong Li
Publication year - 2017
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2017.7362
Subject(s) - artesunate , pharmacology , nephritis , artemisinin , tlr4 , medicine , inflammation , immunology , biology , plasmodium falciparum , malaria
The active ingredient in Artemisia carvifolia, artemisinin, may alleviate inflammation and toxicity. Artemisinin and its derivatives are first‑line anti‑malarial drugs currently, which have rapid effects on fever caused by malaria parasites with fewer side effects. The present study investigated the effects of Artesunate in a mouse nephritis model. Mice were injected intraperitoneally with 500 µl pristine to induce nephritis, and were treated with 28.8 mg/kg Artesunate. Subsequently, proteinuria, renal function, and tumor necrosis factor (TNF)‑α and interleukin (IL)‑6 levels were assessed to evaluate the effects of Artesunate on nephritis. Western blot analysis was used to measure the protein expression levels of α‑smooth muscle actin (SMA), TLR4, myeloid differentiation primary response gene 88 (MyD88), NF‑κB p65 and transforming growth factor (TGF)‑β1 to investigate the underlying mechanisms of Artesunate on nephritis. The results demonstrated that Artesunate reduced proteinuria and preserved renal function in nephritis mice. Artesunate attenuated TNF‑α and IL‑6 levels, suppressed α‑SMA, TLR4, MyD88, NF‑κB p65 and TGF‑β1 protein expression, and decreased caspase‑3 activity in nephritis mice. These results indicated that the effects of Artesunate may prevent nephritis and inhibit inflammation via the TLR4/NF‑κB signaling pathway in mice. Therefore, Artesunate may be a potential therapeutic agent to prevent nephritis.
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